Alzheimer's causes more diverse than previously thought

Researchers have been discovering more
and more about Alzheimer's disease, and some significant progress has
been made in bettering our understanding of the degenerative
condition. Now researchers from Lund University in Sweden have shed
a little more light on the disease, finding that an excessive buildup of amyloid beta isn't solely linked to hereditory factors. The work could lead to more targeted treatment plans for
tackling the disease.

A relatively small percentage of
Alzheimer's sufferers have a hereditary risk gene that causes amyloid
beta to be overproduced in the brain, directly leading to the
condition. In all other cases, the plaque buildup has been
attributed to problems with breaking down and remove amyloid beta,
rather than the body producing too much of it in the first place. The
results of the new study challenge that view, revealing a more
complex picture of amyloid beta's role in the condition.

The new study involved 330 people, with
one group suffering from a mild cognitive disorder that can be an
early sign of Alzheimer's, and a second control group of healthy
individuals. Three different methods were used to test participants,
with the researchers using a PET scanner, performing genetic analysis
and taking cerebrospinal fluid samples.

The results showed an association
between an accumulation of amyloid beta in the brain and high levels
of specific amyloid peptides in the cerebrospinal fluid. According to
the researchers, the link shows that overproduction of amyloid beta,
rather than just problems with disposing of it, can contribute to
development of Alzheimer's in patients, even if they don't have the
hereditary risk gene. In those cases, its thought to be a two stage
problem, with the patient producing too much of the protein, while
also having problems breaking it down.

That knowledge represents yet another piece of the puzzle, helping us to build a more complete picture of the disease. In the long run, the researchers believe that it could help in the development of new treatments.

"The results are important because
they increase the understanding of how Alzheimer's disease arises,"
said Lund University's Oskar Hansson. "Our hope is that this and
other similar studies can increase the possibilities of personalizing
treatments that slow down the disease in the future."